Our center trauma grant continues the hypothesis of our first funding cycle: "Trauma primes cells." This renewal envisions the interweaving of five projects. The clinical core project will continues as a trauma/MOF registry. Pat Offner has noted, however, that a blood transfusion, which we initially used as a surrogate marker of shock, independently predicts MOF. He proposes that lipids in transfused blood prime circulating neutrophils. Gene Moore's project convincingly demonstrated during our first funding cycle that post -traumatic splanchnic hypofusion probably does not translocate bacteria/endotoxin in man. He currently postulates that post-injury gut ischemia primes both circulating neutrophils and distant vascular endothelial cells. Shin Meng's project recognizes the central role of the macrophage in MOF and proposes that liposome encapsulated HSP-72 transfer into macrophages can control their cytotoxic TNF production. Alden Harken postulates that endogenous TNF production by heart directly compromises cardiac function which delays early post- traumatic organ repair and exacerbates late MOF. Ani Banerjee's project postulates that the cell signaling language delineating post- stress/injury priming can be identified and therapeutically manipulated. In addition to a trauma research center, we envision ourselves a trauma research training center.